Illness is a process that everyone experiences repeatedly in one's lifetime.
Until our modern era, illnesses were classified according to their recognizable
signs and symptoms. Today, in addition to the outward appearance of an illness,
we also classify it according to its unique features detectable with the
microscope and with biochemical tests. Thus many illnesses of similar or
identical appearance which were lumped together in the past can now be
distinguished from one another based on their microscopic or biochemical
features. For example, what for hundreds of years was called influenza is now
described as a group of "influenza-like illnesses", each one associated with a
different virus.

On the other hand, many diseases known for centuries and recognizable by their
typical signs and symptoms have been confirmed by modern science to be distinct
entities, i.e. to be associated each with its own particular virus or bacterium
and with no other. Measles, chicken pox and scarlet fever are examples of these.

It has long been known that in some illnesses such as these, one experience of
the illness usually confers lifelong immunity. A second experience with measles
or scarlet fever is extremely rare.

These observations by physicians and patients throughout history, as well as
careful observations of the stages in a patient's recovery >from an acute
inflammatory illness like measles or scarlet fever, have led to certain basic
concepts in medicine.

One of these concepts was formulated as "Hering's Law" in the 19th century,
although it was well-recognized and mentioned by the ancient Greek physician
Hippocrates. This law states that as an illness resolves, its manifest signs and
symptoms travel from the inner vital organs and blood circulation to the outer
surface of the body, often visible as a rash or as a discharge of blood, mucus
or pus. In this way we "throw off" an illness.

Another basic concept arising from the phenomenology of illness, i.e. >from
observations of the directly perceptible behavior of human illness, is the
concept of immunity to or protection from an illness that one has had before.

This immunity to second episodes of certain illnesses like measles or scarlet
fever reveals a knowing function of the human being in relation to illness. This
inner knowing allows us, without any conscious knowledge or effort, to recognize
an illness we've had before and to thereby resist it or quickly repulse it.

Hering's law on the other hand is evidence of an innate doing function of the
human being in healing, i.e. we actively clear the illness from our body, we get
it out of our system as we heal. These inner activities of doing and knowing
work more strongly during illness than in the healthy state, and they were
clearly recognized by the ancient physicians. Hippocrates said illness consisted
of the active element pónos (labor) as well as the passive element pathos
(suffering). Illness is intense inner work. Hippocrates perceived this labor as
a cooking and digesting (pepsis) of our inner poisons during an inflammatory
illness. Today we regard our inner work as a battle against a hostile virus or
bacterium. The all-too-often overlooked point however, is that it is we
ourselves who inwardly, unconsciously determine whether or not to engage in the
battle. The great medical pioneer Hans Selye, M.D., who introduced and
elucidated the role of stress in health and illness explained, "Disease is not
mere surrenderbut also fight for health; unless there is fight there is no
disease (emphasis mine)."1

The symptoms of an acute inflammatory-infectious illness begin not when we are
infected by a virus or bacterium, but when we respond. The magnitude of our
response is influenced not only by the magnitude of the infection, but also by
the inherent strength of what is responding in us. For the ancient physicians
the responder in us was an aspect of our human spirit and our inner vitality;
our inner healing force. Today the physical basis of our inner responder is what
we call our immune system. The phenomenon of immunity hasn't changed, but our
thinking about it has.

The severity of the early symptoms of a particular illness is directly
proportional to the vigor of our immune response and indirectly to the burden
and noxiousness of the infection to which we are responding. The surprising fact
is that most of the symptoms of an infectious disease are caused not by the
germs themselves but by our own activity of the immune system in fighting the
germs. The germ "invasion" of our body is often silent, and can take place
gradually over a long period of time without disturbing us. It is only when our
immune system decides to do battle with the encroaching germs that we start to
feel sick.

The metaphor of battle is a convenient, but not fully accurate description of
the relationship between our immune system and the proliferating viruses or
bacteria during an acute inflammatory/infectious illness. Pasteur's germ theory
assumes that disease germs have a predatory nature: that they prey on our flesh
for their own survival, while contributing nothing to us in return. The germ
theory further assumes that the harmful or lethal effects of
infectious/inflammatory diseases are a direct result of this predation of the
human body by germs.

In early microscopic studies of host tissues in acute inflammatory/infectious
diseases, Pasteur, Koch and their colleagues repeatedly observed that germs were
proliferating while many host cells were dying. They made the critical
assumption, upon which all further thinking has been based, that the germs
attack and destroy otherwise healthy cells, thus causing direct harm to the
human body.

It would have been equally justified by the observable facts to assume that the
cells were dying for inapparent biochemical reasons and that the proliferating
germs were attracted to the site of increased cell death and decay just as
flies, crows and vultures are attracted to death in outer nature. A choice was
available early on between regarding germs as predators and regarding them as
scavengers. The nineteenth-century thinking of the time was captivated by the
Darwinian images of "Nature red in tooth and claw" and the relentless struggle
for survival. The decision to see germs as predators was perhaps inevitable, and
that has made all the difference in our current thinking about illness and
health. That early decision by Pasteur and his followers led to medicine's
present nearly-exclusive focus on combating germs, while neglecting all the
subtle but far-reaching ways to strengthen the host against lasting harm from
inflammatory/infectious illness.

Just as flies, crows and vultures were regarded by the Native Americans as
playing a necessary and helpful role in the great chain of Being, so too with
germs which scavenge death and decay within our bodies. The true causes of
inflammatory/infectious illnesses will ultimately be found to reside not in the
germs, but in the various human frailties which allow the forces of death and
decay to predominate in us. The scavenging germs are the markers of our waxing
and waning states of physiologic imbalance when cell death and decay temporarily
exceed their normal limits.

The metaphor of battle between immune system and germs is justified provided we
remember that our real enemies are the forces of death and decay. The germs
themselves become sacrificial victims marked for destruction by our immune
system because their role is to absorb the products of death and decay. Germs
become poisonous to us through embodying the poisons we create. In "battling"
germs, the real battle is to overcome ourselves and to refine our nature. This
concept is implicit in the following discussion of how our immune system does
battle with germs.

Using battle as our metaphor, we can imagine three possible scenarios. In the
first, the attacking army is not strong, but the defenders are, and the
attackers are routed from the field in a bloody but one-sided and brief battle
in which the defenders suffer no casualties. This describes a typical case of a
benign but acute inflammatory-infectious illness like roseola which usually
expresses itself in a very high fever of 105° or 106°F and an extensive rash
despite being no threat whatsoever to the host.

A second scenario would be when the opposing armies are evenly matched and there
is a fierce battle with many casualties on both sides. This could describe an
acute life-threatening inflammatory illness like septicemia or an overwhelming
pneumonia, in which recovery or death is equally likely.

In the third scenario, the war reporter arrives late at the battlefield and
finds no carnage, in fact little or no evidence of any previous battle. The
defending army is quiet and no attackers can be seen. The reporter at first
concludes that it was a very quick and easy victory for the defenders and the
attackers have fled. On closer investigation, however, he finds that no battle
took place because the defenders were unable or unwilling to fight. What our
reporter at first thought was the defending army in reality consists of
non-combatant defenders who have been quietly and massively infiltrated by the
attackers. The attackers blend in, occupying the defenders' homeland, and any
defenders who would fight them have gone underground where they intermittently
harass and provoke the occupying enemy.

The point of this elaborate metaphor is to demonstrate by analogy that the
absence of fevers and other symptoms and signs of inflammatory illness (the
absence of a battle) does not always mean that our immune system (the defending
army) has been victorious!

Today it is more often the case that when we don't fight our battles vigorously
and often enough, i.e. when our fevers and discharging inflammations are very
seldom and mild, then we are liable to be infiltrated by the enemy in disguise
and suffer from chronic allergic or autoimmune disorders. This concept today is
called the hygiene hypothesis. In the 1920's Rudolf Steiner expounded
essentially the same concept as a mutual interplay between opposing forces of
inflammation and of sclerosis, in which the healthy state is a dynamic balance
between the two.

Returning to our third scenario, there are of course times when the absence of a
battle, i.e. absence of obvious disease symptoms, indeed does mean that the
defending army has easily routed the enemy and is truly immune from further
attack. Thus we see that two entirely opposite outcomes, 1. immunity from attack
and 2. quiet infiltration by the attackers into the defenders' homeland (the
host body) can have the exact same appearance superficially. This analogy
applies precisely to another pair of similar-appearing but inwardly opposite
states, i.e. the true immunity conferred by overcoming illness as opposed to the
apparent immunity conferred by vaccination. In both cases the host appears to be
healthy due to the absence of illness, but true health is much more than the
absence of overt illness. We will illustrate this point further when we discuss
smallpox in part 3.

To complete our phenomenological description of immunity, we must note that in
addition to the functions of clearing illnesses from the body and of recognizing
the illnesses it has previously encountered, the immune system has another
cognitive or knowing capacity. This is the discrimination of self from non-self
and the ability to "tolerate", i.e. to not treat as foreign and to not react to,
any elements of self. This remarkable knowing of the immune system also extends
to its ability to tolerate, in pregnancy, a massive foreign presence in the
body, the fetus, without reacting to it at all.

Thus we see the incredible skill and apparent purposefulness of doing and the
discriminating capacity of knowing possessed by the immune system. Although
modern science rarely uses the words "knowing" and "doing" in its descriptions
of the immune system, nevertheless distinct knowing and doing functions are very
clearly and unavoidably implied in all scientific writing on immunology. Science
prefers to focus on the molecular level, hoping to find in molecular events the
elusive key to understanding, if not why, at least how the immune system does
what it does.

Today the immune system is most often described in articles and textbooks as
comprising those bodily organs, cells and functions which discriminate between
self and non-self. The molecules of self or non-self which the immune system can
recognize are called antigens. One branch of the immune system, called the
humoral immune system, consists primarily of antibodies which are protein
molecules made by the body to specifically interact with foreign antigens.
Antibodies attach themselves to any foreign antigens like bacteria or parasites
which may exist in blood or body fluids outside of the body's cells. Antibodies
are attracted to such extracellular antigens and usually coat these antigens as
one step in the complex process of the destruction, digestion and elimination of
foreign matter in us by our immune system.

We come now to a beginner's question, one seldom or never asked in the science
of immunology. It is, why does our immune system work in such an inconsistent
way, providing for permanent immunity from recurrence only after certain
illnesses and not after others? A "why" question such as this is usually
considered irrelevant in modern science, while the equivalent "how" question is
actively pursued. In the case of immunity to illness, it is the "how" questions
that have led science to the idea and the practice of vaccination.

For science the pertinent question is, how can we imitate nature and bring about
lifelong immunity to an infectious-inflammatory illness, but without having to
experience the illness first? The first task would be to learn exactly how
nature itself manages to maintain permanent immunity in us after a first
experience of illness. What is this process of lifelong maintenance of
resistance to a particular illness? Can science duplicate it?

It is an interesting fact that sometimes a practical scientific breakthrough
happens out of an intuition, a hunch, long before the discoverer or anyone else
is able to explain just how and why this particular breakthrough works. This is
true of the work of Jenner and Pasteur, the great initiators of the practice of
vaccination. Astoundingly, in our modern era when vaccinations are so widely
acclaimed and practiced, science still cannot explain how they work.

In the New Scientist magazine of May 27, 2000, an article on AIDS vaccine
research quotes the following from two scientists: "I'm amazed by the amount of
basic science we don't know," and "the assumption that successful vaccines work
by simply producing antibodies is almost certainly wrong." The article then
describes how one vaccine researcher found that in a certain viral disease of
horses, vaccination was successful in inducing antibodies against the virus,
nevertheless the vaccinated horses died faster than the unvaccinated ones!
Referring to our present ignorance as to just why these vaccinated horses would
succumb, he stated, "It's an issue people haven't wanted to think about, but we
might have to."

Vaccine science and practice have always been based on certain assumptions,
which we are only now beginning to examine. One of these is that antibodies in
the blood (humoral immunity) confer protection against an illness, and that the
level of antibodies correlates with the degree of protection. This relationship
between measurable antibodies in the blood and apparent protection >from illness
has been observed for decades in many types of infectious diseases. It is not
known however whether the antibodies persisting in the blood for months or years
after an infectious disease are themselves responsible for protecting us from
recurrences of that disease or whether they are merely markers of a protection
that is accomplished by another part of the immune system. It is also not known
whether the apparent protection associated with vaccination-induced antibodies
is a benefit pure and simple or whether a hidden cost to the immune system is
involved. The idea of a hidden cost is considered unthinkable by vaccine
researchers for obvious practical reasons, yet it continues to be a nagging
doubt among an ever-widening circle of parents, consumer advocates,
chiropractors, holistic physicians and other discerning people.

The AIDS research quoted at the beginning of this article suggests that it's not
the antibodies which protect us, but rather it's the cellular immune system.
Also called the cell-mediated immune system, it comprises the white blood cells,
all the lymph nodes and lymphatic tissue throughout the body and is concentrated
in the thymus, tonsils, adenoids, spleen and bone marrow. It is generally agreed
that the primary function of the cellular immune system is to destroy foreign
intracellular antigens like viruses and some bacteria as well as the cells that
harbor them. This is accomplished by the various white blood cells which are
able to move inside, outside and through the walls of our blood vessels and to
access every part of the body.

In the past I have been tempted to assign the immune system's doing function to
the cell-mediated branch and its knowing function to the humoral
antibody-mediated branch. This neat division of function is not borne out by the
facts. Research shows us that each branch participates in functions of both
knowing and doing, although most of the immune system's muscle to destroy,
digest and drive out intruders is flexed by its cell-mediated branch. Thus,
while immune system functions of knowing and doing may be conceptually distinct,
in the physical reality they are overlapping in an exceedingly complex
orchestration of organs, cells, molecules, hormones and chemical messengers.

There are also other aspects of the immune system which are beyond the scope of
this article. Reading a modern textbook of immunology can be frustrating as one
finds a bewildering array of cellular, molecular and antibody-mediated processes
which science has discovered without knowing how they all fit together and
manage to cooperate in health and in illness in the human being. It's something
like hoping to find an understanding of how an automobile performs by studying
its disassembled parts in an auto parts shop.

At the present time, it is thought that the encounter between self and non-self,
that is, between the immune system and a foreign "invader" like a virus or
bacterium begins in the domain of the cellular immune system with a cell called
the antigen-presenting cell. If the foreign guests are not great in number or in
their noxiousness, the cellular immune system is able to dispatch them, digest
them and clear them from the body without ever calling into action its coworker
the humoral or antibody-mediated immune system. This explains the very important
fact that without our awareness we are continually infected with many small
numbers of different germs in our body, some of them nasty, and the cells of our
immune system continually shepherd them and keep them in check without the
assistance of antibodies.

Like dust and other unseen debris, these microorganisms enter our bodies as we
breathe, eat and drink. Only when the number or rate of growth of germs exceeds
a certain threshold are they then recognized by the humoral immune system,
resulting in the formation of antibodies specific to the particular provocative
bug. At this stage we may have only mild fleeting symptoms or none whatsoever.
This explains how we may be found to have antibodies against illnesses we don't
remember ever having had! This is called "subclinical infection", i.e. infection
without symptoms, and it happens commonly.

Thus science has discerned three levels of infection. The lowest level is our
steady-state equilibrium of everyday life in which we peacefully co-exist with
our inner menagerie of germs without needing to form detectable antibodies
against them. At this lowest level our cellular immune system is quietly busy
keeping our bugs in line and when necessary pruning the flock. Thus, although
small numbers of disease agents are within us, out cellular immune system sees
to it that we remain well and free of disease symptoms, and that our germs are
under control.

At the second level of infection, we temporarily relax our vigilance and allow a
certain group of germs to begin rapidly multiplying to the point where the
humoral immune system is alerted and begins to produce antibodies against the
offending bugs. This sets off a cascade of immune system functions which succeed
in fairly quickly quelling our rebelling germs, so quickly that the person
hosting all these inner happenings is unaware of having just gone through a
subclinical illness. The identity of the wayward germ can afterwards be
diagnosed by the presence in the blood serum of the specific antibodies produced
against it by the humoral immune system.

At the third level of infection things get seriously out of control and all our
inner alarm bells go off as a tribe of germs proliferates wildly and provokes
the full defensive reaction of our immune system. This is called the "acute
inflammatory response", which usually includes fever, release of stress hormones
by the adrenal glands, increased flow of blood, lymph, mucus, and a streaming of
white blood cells to the inflamed area. The human host of these wisdom-filled
events now feels sick and may experience pain, nausea, vomiting, diarrhea,
weakness, chills and fever. We have now emerged from the realm of the
subclinical to a full-blown clinical illness, with all of its intense and often
frightening symptoms. It is critical to a healthy understanding of these things
to realize that we never merely suffer through an illness in a passive,
one-dimensional way. In an acute illness, parts of us that in health are most
active, like our mind and our muscles, are subdued, while other parts like our
blood, glands and immune system are much more active than normal. Thus every
illness rouses us to become more inwardly active than usual, and this inner
activity of ours is the cooking through, the sweating out and the throwing off
of the illness. This is hard work, and every illness calls upon and exercises
capacities in us which otherwise would have remained dormant. Adults often
notice these new capacities as a change in attitude or outlook after an illness.
Children often manifest positive changes in their behavior or development after
overcoming an acute inflammation or fever.

Having successfully passed the challenge of a particular illness, we may not
need to experience it again. Something about the illness and our response to it
has made us immune to its recurrence. If we knew what that something was,
perhaps we could learn how to use it to create health and prevent illness. Of
course, this is the basic concept of vaccination, but the all-important question
is, does vaccination accomplish what we think it does?

We've already suggested that it's probably the cellular immune system, and not
antibodies, which protect us against illness. Surely antibodies can have no role
in either preventing or overcoming first bouts of infectious-inflammatory
illness, because they are formed only after the illness has peaked. It must be
the cellular immune system which confers the resistance to, as well as the
capacity to overcome, both first episodes and subsequent episodes of infectious
disease. To understand how this might happen, it is helpful to examine more
closely the very illness and its vaccination which started the whole debate:
smallpox.

That vaccines can confer a degree of protection from certain
infectious-inflammatory illnesses is clear. What is not clear, as mentioned
earlier, is exactly what vaccinations do to the immune system to bring about
their protective effect. Researchers generally agree that vaccines do not
prevent the particular virus or bacterium from entering the body nor from
beginning to multiply within it. It is thought instead that the vaccines
stimulate or "prime" the immune system to quickly eradicate the offending germ
soon after it begins to infect the host.

Let us consider how this process might work in the case of smallpox. Our
knowledge about smallpox and its vaccination is based on over 200 years of study
of this dramatic and much-feared illness by physicians in many countries.

The natural course of the illness begins when one "catches" smallpox from
someone with a smallpox rash or from the mucus or pus of smallpox on a patient's
bedclothes or dressings. For the next twelve days there are no signs or symptoms
at all and the new patient is not contagious even though the smallpox virus is
multiplying within the body. On or about the twelfth day large numbers of
smallpox virus enter the blood (viremia) and the "toxemic" phase of the illness
begins, meaning a poisoning or contamination of the blood circulation. This
blood poisoning of smallpox is the beginning of the overt illness, with symptoms
of fever, prostration, severe headache, backache, limb pains and sometimes
vomiting. After three or four days of these symptoms the typical smallpox rash
begins to erupt and in the next one to two days the fever falls to almost normal
and the patient feels much better.

The skin eruption begins as red spots which over the next few days evolve into
raised pimples, which then change to blisters which then become pus-filled
(pustules). On the 11th to 13th day of the illness the pustules begin to dry up
and form crusts or scabs which then fall off by the end of the third week of the
illness. The fever usually returns, less severely, after the pustules appear and
then becomes normal as the crusts and scabs form. If one dies from smallpox, it
may be in the first week of the illness if the toxemia is very severe, but most
smallpox deaths have occurred toward the end of the second week after the
pustules appear.

The majority of smallpox patients survive, and the falling away of the dried-up
scabs from the skin signifies the final stage of healing, approximately 33 days
after catching the infection. The dramatic course of smallpox illustrates very
well some of the concepts discussed earlier in this article. The twelve-day
incubation period during which the smallpox virus actively multiplies in the
body without provoking the slightest symptom confirms the point that it is our
response to infection, not the infection itself, which causes the typical
disease symptoms of fever, aches and pains and extreme weakness.

The fact that the fever drops and the patient feels much better after the rash
breaks out illustrates Hering's Law. The poisons circulating in the blood during
the toxemic phase cause the most severe symptoms of smallpox. These symptoms
improve considerably once the blood clears out its poisons by discharging them
through the skin, producing the typical pus-filled blisters of smallpox. The
chief danger of smallpox consists in the degree of blood poisoning and in the
huge and exhausting effort required for the immune system to push the poisons
out of the blood and through the skin. When the toxemia, the poisons, are
overwhelming and the patient lacks the strength to discharge them out of the
body, then the patient may die in the effort, either before the eruption ever
appears or else, utterly spent, afterwards.

The patients who survive smallpox will have lifelong neutralizing antibodies to
smallpox virus in their blood and permanent immunity to a second episode of the
illness. What does this mean?

Using the battle metaphor from part one, we could say that the victorious
defending army has acquired much valuable skill, know-how, and confidence
through its combat experience as well as certain medals awarded to acknowledge
their participation in combat. The first three attributes are comparable to the
inner strengthening of the cellular immune system which is attained through
overcoming an illness like smallpox. The medals as visible tokens of achievement
are roughly comparable to the antibodies visible on simple blood tests
indicating that the host has already won that battle and is likely to be immune
to future attacks of the same illness.

If a foolish general were under the illusion that merely wearing a combat medal
actually conferred the know-how, skill and confidence gained in battle, then he
might propose pinning medals on soldiers with no combat experience to make them
immune to dangerous future battles. That would bestow the same outward
appearance to the seasoned and unseasoned soldiers alike, belying their
experience.

In the same way, science bestows antibodies through vaccination and mistakenly
assumes that it is bestowing the immune strength that can only be developed
through the experience of illness. In equating the significance of
vaccine-induced antibodies with that of illness-induced antibodies, science
confuses the outer sign of the battle experience with the experience itself.
Antibodies arising through illness are markers of immunity and (unlike the
medals in our battle metaphor) also contribute to immunity, but antibodies alone
are not sufficient to confer lasting immunity to a particular illness. There are
several diseases which may recur repeatedly, such as herpes outbreaks, despite
high antibody levels. The evidence suggests that it is our cellular immune
system which confers lasting immunity, with antibodies playing a secondary role
in the process.

Immunity is really the result of our experience, of having gone through, along
with our cellular immune system, an active process (the combat in the metaphor)
of learning and strengthening. The immune system is a limb of us, and it learns
from experience just as we do. Antibodies signify that we've had experience of
illness, often repeatedly, but not necessarily that we've gained anything from
the experience. When on some level we respond with greater initiative to our
experience of illness, actively processing, digesting and ultimately learning
from such experience, then we are usually immune from having to repeat it. In
such cases our cellular immune system has strengthened itself through its active
encounter with, and overcoming of, the illness. In this view, immunity is the
result of having successfully met the challenge of a particular illness and
having gained mastery over it. It is like learning a particular skill, such as
riding a horse, which is then usually retained for life. On the physiologic
level, the skill and mastery we gain in overcoming illness accrue to our
cellular immune system.

This active process of acquiring mastery cannot be replaced by a vaccination
unless the host's immune response to the vaccination is essentially identical to
its response to the illness itself, even though reduced in intensity. This would
mean that in order to produce genuine cellular immunity, a vaccination would
have to reproduce the experience of the illness, causing some of the same signs
and symptoms, though milder, that are caused by the illness. To see if this is
true, let us look at smallpox vaccination.

The vaccination consists of introducing live cowpox (vaccinia) virus into the
skin by multiple superficial punctures in a small area about 1/8 inch diameter
on the upper arm. The vaccination site is then inspected twice after 3 and 9
days to determine if the vaccination "takes" or not. A primary reaction or
"take" evolves as follows: for three days after the vaccination there is no
reaction whatsoever. On the fourth day a small red pimple appears which
gradually grows into a blister which becomes pus-filled, surrounded by a zone of
redness and often with tender, swollen glands in the armpit and mild fever. This
reaction peaks on the 8th to 10th day, after which the pustule gradually dries
up and forms a scab which eventually falls off leaving a scar.

Clearly the primary "take" reproduces the experience of smallpox itself
described earlier, but of course in a very limited way so as to generate only
one pock rather than many dozens of them. The cellular immunity produced by
smallpox vaccination is also limited, lasting from six months to three years.
This immunity probably coincides with the length of time that the exercised
"muscle" of the cellular immune system remains strengthened from its labor of
discharging the single cow pock resulting from the vaccination. The antibodies
appearing in the blood after primary smallpox vaccination may remain for over
ten years, but these antibodies cannot be taken as a trustworthy sign of
immunity. The official description of the currently available smallpox vaccine
in the U.S., which was manufactured by Wyeth Laboratories, states vaguely "the
level of antibody that protects against smallpox infection is unknown"2 If we
can state blandly that the protective level of antibody is still unknown after
having assumed for several decades that protection is directly correlated with
antibody level, then surely it is time to rethink that assumption.

In practice antibody levels were seldom used in the smallpox era as a measure of
immunity. Anyone not vaccinated in the previous three years was considered to be
susceptible to smallpox, regardless of their antibody level.

The all-important question is how to interpret the meaning of reactions to
smallpox vaccination which are milder and briefer than the primary "take" which
peaks in ten days, and which does result in a genuine though short-lived
immunity of the cell-mediated system.

Since the early 1970's only two types of reactions to smallpox vaccination have
been officially recognized, as recommended by the World Health Organization
(WHO). For purposes of greater clarity, in this discussion I will be referring
to the older classification which recognized three types of normal reactions to
smallpox vaccination.

The second type of normal skin reaction to smallpox vaccination was called the
accelerated or vaccinoid reaction, usually in people who had some immunity to
smallpox at the time of vaccination, either from a previous experience of the
disease or from a previous smallpox vaccination. In the accelerated reaction,
the skin blister which forms is smaller and reaches its maximum size and
intensity between the 3rd and 7th day after the vaccination. This reaction works
in exactly the same way as the primary reaction but to a lesser degree, boosting
the cell-mediated immunity that is already present, but waning, from the
previous vaccination.

It is the third type of reaction to smallpox vaccination that in my opinion has
created all the problems, that has been at the root of a 200 year old
controversy over the usefulness of smallpox vaccination. This stems from the
fact that this reaction for years was interpreted as indicating immunity to
smallpox, when it often meant exactly the opposite. In many cases the bearers of
this reaction may have had a suppressed cellular immunity, making them on
repeated revaccination more susceptible to smallpox than an unvaccinated person!

This third type of reaction to smallpox vaccination was originally called an
immune reaction, then later renamed an early or immediate reaction. A small
pimple forms at the vaccination site which may evolve into a tiny blister,
peaking on the second or third day and diminishing thereafter. An earlier
textbook of viral diseases >from the smallpox era states the following: "The
early or immediate reaction is an indication of sensitivity to the virus and may
be given by persons who are either susceptible or immune to smallpox.[It] cannot
be regarded as a successful result and cannot be guaranteed to induce or
increase the person's resistance to smallpox."3 This is a typical scientific
understatement that glosses over years of devastating results of smallpox
vaccination in which thousands of vaccinated people who were thought to be
immune based on their so-called "immune reaction" to vaccination later caught
smallpox and died.

Ian Sinclair, writing on the history of smallpox, states:

"After an intensive four-year effort to vaccinate the entire population between
the ages of 2 and 50, the Chief Medical Officer of England announced in May 1871
that 97.5% had been vaccinated. In the following year, 1872, England experienced
its worst ever smallpox epidemic which claimed 44,840 lives.In the Philippines,
prior to U.S. takeover in 1905, case mortality [death rate] from smallpox was
about 10%.In 1918-1919, with over 95% of the population vaccinated, the worst
epidemic in the Philippines' history occurred resulting in a case mortality of
65%.The 1920 Report of the Philippines Health Service [stated] 'hundreds of
thousands of people were yearly vaccinated with the most unfortunate result that
the 1918 epidemic looks prima facie as a flagrant failure of the classic
immunization toward future epidemics.'"4

How can this be? How can these historical facts be reconciled with my earlier
statement that a primary take in response to a first smallpox vaccination
results in genuine cellular immunity for up to three years? The usual
explanation offered is that the vaccine used was inactive due to loss of potency
in storage, but this clearly cannot be the whole answer to the many documented
instances of failure of smallpox vaccination to protect from smallpox.

The answer is an open secret which has been very well known for years, but never
fully understood: that many first recipients of smallpox vaccine fail to produce
a take (primary reaction) and continue to fail to do so even when revaccinated
many times. The textbook states,

"Easton (1945) records of one man who died of confluent smallpox that
vaccination had been attempted at birth, again in 1941 and ten times in 1943
without a take, thus emphasizing the danger of accepting even repeated
unsuccessful vaccination as evidence of insusceptibility to smallpox.."5

This is an excellent example of a vitally important observation leading to an
irrelevant, though not incorrect, conclusion. This example begs the question:
how many repeated failures to react does it take to justify the concern that
continuing to revaccinate may be doing more harm than good?

The relevant conclusion, in my opinion, is that due to differences in immune
response capability among individual human beings at the time of first
vaccination, in some individuals the cellular immune system lacks the muscle to
push out the single pock eruption that is the primary take. The scratching of
the virus into the skin of the arm is a strong challenge to the immune system. A
successful take depends on the ability of the cellular immune system to respond
to that challenge in an equally vigorous way, to push the intruding virus right
back out of the body. It is a simple matter of action and reaction, of challenge
and response. If Charles Atlas challenges a 97-pound weakling to arm wrestling
and his opponent's arm immediately collapses, we would not think that the
challenge ought to be repeated indefinitely if the weak condition of the
responder had no means of improving! Yet in thousands of individuals in the last
200 years who may have been weakened through stress, poor nutrition and poverty,
whose cellular immune systems were not vigorous enough to respond to smallpox
vaccination with a take, the effect of repeated revaccination, which was
commonly practiced, was to weaken these individuals' immune systems still
further, making them no doubt more vulnerable to smallpox than they had been
before vaccination! This would explain the disastrous results of the
above-mentioned smallpox vaccination campaigns in England, the Philippines and
in many other countries as well.

The ambivalent nature of the early reaction to smallpox vaccination is analogous
to the third battle scenario mentioned in part one of this article. When little
or no signs of battle (reaction) are visible, it may mean that the defenders
were easily victorious (the host is immune) or contrariwise it may mean that the
defenders lacked the strength to fight and their homeland was subsequently
quietly infiltrated by the attackers. When a smallpox vaccine recipient lacks
the immune muscle to respond to the viral intrusion of his or her body with a
vigorous pock-forming discharge, then we might expect that most of the intruding
virus has remained in the body. With each revaccination the burden of vaccinia
virus in the body increases, and the suppressive effect of this viral burden on
the cellular immune system also increases, eventually resulting in a dangerous
state of immunosuppresion. This may also explain the occasional catastrophic
effects that were observed resulting from a brief medical fad in the 1970's:
treating recurrent herpes infections with repeated smallpox vaccinations.

The disease smallpox and its vaccination are fruitful subjects to study in order
to understand how the immune system works, because we can observe what happens
on the skin as vital clues to what might be happening inside the body. The main
lesson from this study is the exceedingly important fact that a lack of a
vaccine reaction, and by extension a lack of illness symptoms, can by no means
be taken as a sign of immunity or of health.

The other critical fact confirmed by our historical experience with smallpox
vaccination is that individual differences in response to vaccination are
extremely important. One size most definitely does not fit all. It is clear that
although the smallpox vaccine was effective in conferring a temporary immunity
in some individuals, an unknown number of other individuals were probably harmed
by the vaccine. With the smallpox vaccination the adverse effects were fairly
obvious, they often appeared on the skin. With other vaccines in use today the
adverse effects may not be so obvious. We've seen with smallpox that the same
vaccination procedure which temporarily strengthened the cellular immune system
in some individuals probably weakened it in others, especially upon repeated
revaccination.

The possibility, that the up to 39 doses of 12 different vaccines which children
today receive by school entry may be impacting the cellular immune systems of
many individual children in a negative way, suggests itself to the open mind.
Science has most of the knowledge and the tools it needs to investigate and to
find answers to these unanswered questions. All it needs now is the will. May it
come soon, for our children's sake.